This antibody is purified through a protein A column, followed by peptide affinity purification.
Immunogen
This DCLK2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 167-196 amino acids from the N-terminal region of human DCLK2.
Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.
Konservierungsmittel
Sodium azide
Vorsichtsmaßnahmen
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Lagerung
4 °C,-20 °C
Haltbarkeit
6 months
Dijkmans, van Hooijdonk, Fitzsimons, Vreugdenhil: "The doublecortin gene family and disorders of neuronal structure." in: Central nervous system agents in medicinal chemistry, Vol. 10, Issue 1, pp. 32-46, (2010) (PubMed).
Kerjan, Koizumi, Han, Dubé, Djakovic, Patrick, Baram, Heinemann, Gleeson: "Mice lacking doublecortin and doublecortin-like kinase 2 display altered hippocampal neuronal maturation and spontaneous seizures." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 106, Issue 16, pp. 6766-71, (2009) (PubMed).
Gorelik, Sapir, Reiner: "Gene trapping: an antibody-dependent approach for verifying integration in your favorite gene." in: Cellular & molecular biology letters, Vol. 13, Issue 4, pp. 614-20, (2008) (PubMed).
This gene encodes a member of the protein kinase superfamily and the doublecortin family. The protein encoded by this gene contains two N-terminal doublecortin domains, which bind microtubules and regulate microtubule polymerization, a C-terminal serine/threonine protein kinase domain, which shows substantial homology to Ca2+/calmodulin-dependent protein kinase, and a serine/proline-rich domain in between the doublecortin and the protein kinase domains, which mediates multiple protein-protein interactions. The microtubule-polymerizing activity of the encoded protein is independent of its protein kinase activity. Mouse studies show that the DCX gene, another family member, and this gene share function in the establishment of hippocampal organization and that their absence results in a severe epileptic phenotype and lethality, as described in human patients with lissencephaly. Multiple alternatively spliced transcript variants have been identified.